Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

OSCE Neuro Remediation > CVA > Flashcards

CVA Flashcards

1
Q

What is a CVA?

A

Cerebralvascular Accident (Stroke) is and acute onset of neurological dysfunction resulting from a an abnormailty of normal cerebral blood supply. The disruption must last atleast 24 hours or result in death with that 24 hours.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the 2 types of CVA?

A
  • Ischemic (lack of blood from thrombus formation, embolus, or low perfusion)
  • Hemorrhage (rupture of blood vessles)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What percentage of strokes are ischemic vs. hemorrhagic?

A

87% ischemic vs 13% hemorrhagic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the etiology of ischemic strokes?

A
  • Atherosclerosis is primary factor
  • Something causes tear or break in intimal lining
  • Interruptions of blood flow occur at at areas of bifurcation, constriction or angulation of artery
    • Turbulent flow or piece of thrombus breaks off and travels to narrow spot in the vessels ( could be due to CVD [rheumatic fever, MI, arrhythmias, CHF, Endocarditis], DVT; fat tumor, or air emboli)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

At what point will symptoms of Ischemia appear?

A

70-75% occlusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the 2 types of hemorrhagic stroke?

A

10% are intracerebral, 3% are subarachnoid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What causes hemorrhagic stroke?

A

Factors that weaken walls of arteries or increase pressure on them such as atherosclerotic plaques and Developmental abnormalities

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the developmental abnormalities?

A
  • Berry aneurysms
  • Arteriovenous Malformations (AVM
    • tangle of arteries and veins having no capillary system between them
    • dilate and weaken over time
    • Rupture in 50% of cases
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are nonmodifiable risk factors?

A
  • Race (african american at higher risk)
  • Increasing age
  • Gender (male)
  • Heredity
  • previous stroke
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are modifiable risk factors?

A
  • HTN (especially above 160/95)
  • CVD
  • Diabetes
  • TIA
  • Hyperlipidemia
  • Smoking
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Different types of CVD that contribute to stroke

A
  • CHD (Coronary Vascular disease)-athersclerosis/MI
  • CHF- heart unable to keep up with pumping blood
  • Valvular disease- damaged valves
  • Arrythmias (a-fib)-pooling of blood and increase risk of emboli
  • Cardiac surger- clamps on aorta, athersclerosis can form
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

T/F Diabetes increases risk of hemorrhagic stroke

A

False, increase riske of ischemic stroke

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Percentages on TIAs in relation to CVA:

A
  • Only 10% stroke preceded by TIA
  • 36% of people who get TIA will get stroke in 5 years
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How do you prevent a stroke?

A
  • Control modifiable factors
    • Smoking, hyperlipidemia
    • Dietary control to avoid diabetes and heart disease
    • Keeping BP under control
  • Awareness of signs/sxs of CVA
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the signs/sxs of CVA?

A
  • sudden severe headache of unknown cause
  • Sudden weakness or numbness of the face, arm, leg, on one side
  • Sudden dimness of loss of vision, especially in one eye
  • Unexplained dizziness, unsteadiness, sudden falls (especially with the other sxs)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

T/F early recognition, especially with an ischemic stroke, can reduce morbidity

A

True

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the pathophysiology?

A

Loss of blood supply results in death to core of brain cells (infarction)⇒Core surrounded by metabolically lethargic cells (penumbra)⇒Necrosis of core causes cascades of chemical activity that can further damage cells⇒Edema occurs soon after infarct

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Facts about Edema

A
  • Peaks within 3-4 wks
  • usually gone within 3 wks
  • Can increase ICP and cause brain shift
    • Caudally = brainstem herniation
    • CL= midline shift
  • Most frequent cause of death in acute CVA
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are anatomical Considerations?

A
  • 80% occlusion before generally required before sxs develop
  • Factors that determine sxs:
    • Location
    • Size of infaract
    • Presence of collateral circulation (slowly developing occlusions)
    • BP-increased pressure stretches arteral wall
      • produces contraction of smooth muscle and narrowed lumens-decreased blood flow
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are lacunar infarcts?

A

small infarcts usually <15 mm in diameter. They result from occlusion of small penetrating arteries damaged by chornically elevated arterial BP. Multiple infarcts can result in problems.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are the types of syndromes? which is most common?

A

PCA, ACA, MCA; MCA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Where does damage from ACA syndrome occur?

A
  • Primary motor cortex and Internal Capsule = paresis to of LE>UE and face (blood supply into superior medial side of face)
  • Primary sensory cortex= sensory impairements LE>UE
  • Uncertain of localization = mental impairments (perseveration, confusion, amnesia)
  • Superior frontal gyrus = urinary incontinence
  • Corpus Callosum = difficulty with imitation and bimanual tasks, apraxia
23
Q

Where does damage from MCA syndrome occur?

A
  • PMC and internal capsule = paresis to CL face, UE and LE (LE the least)
  • PSC and int. capsule = sensory damage to face, UE, LE
  • Broca’s aphasia
  • Wernicke’s aphasia
  • Sensory assoc. cortex = perceptual deficits (neglect, apraxia, depth perception)
  • Optic radiation in int. capsule= homonymous hemianopsia
  • Frontal eye fields or descending tracts = loss of conjugate gaze of opposite side
  • Parietal lobe (SSA) = sensroy ataxia of CL limb
24
Q

Where does damage to PCA peripheral territory occur?

A
  • Primary visual cortex = CL homonymous Hemian.
  • Visual assoc. cortex = prosopagnosia
  • Dominant calcarine lesion and posterior part of corpus callosum = Dyslexia w/o agraphia
  • Inferomedial temporal Lobe = memory deficits (short term into long term)
25
Q

Where does damage to PCA centeral territory occur?

A
  • VPL of thalamus = Thalamic syndrome (sensory, impairments and spontaneous, intractable pain)
  • Subthalamic nulceus = involunary mvmts (coreathetosis, hemiballismus)
  • Cerebral peduncle in midbrain = CL hemiplegia
  • CN 3 and cerebral Peduncle
26
Q

What is the first thing you need to do correctly diagnose a stroke? What are signs/sxs that produce caution with stroke as dx?

A

Exclude other possibilities

  • Signs/sxs
    • Gradual onset of sxs
    • No focal neurological signs
    • Fluctuating neurolgical signs
    • unexplained fever
27
Q

What is the next step in dx? Why? What is the best way to determine dx?

A
  • Determine if it is hemorrhagic or ischemic
  • If ischemic= must be given tPA
  • CT is best way (must be done within 3 hours of stroke to find ischemic or tPA won’t work)
28
Q

What are direct iimpaiments associated with stroke?

A
  • Sensory deficits
  • Pain
  • Visual Deficits
  • Motor deficits
  • Motor programming deficits
  • Speech and Language disorders
  • Dysphagia
  • Perceptual Dysfunction
  • Cognitive Dysfunction
  • Affective disorders
  • Behavioral Changes
29
Q

Sensory Deficits:

A
  • 50% of cases
  • Can be loss of any sensation (44% propioception, leads to sensory ataxia)
  • Depdends on size and location
    • Local loss = coritcal damage
    • Widespread loss = thalamic injury
      • neglect and risk of self-injury
30
Q

Pain:

A
  • headaches
  • If PCA involved = Thalamic Sensory syndrome
    • severe, continuous pain
    • Exacerbated by input from innocuous stimulus
    • does not appear right away (takes wks/mos)
31
Q

Visual deficits:

A
  • Homonymous hemianopsia-results from destruction of Optic radiation (MCA) and primary visual cortex (PCA),in 25% of CVAs,Can be factor in neglect
  • Dipolplia- due to defective function in extraocular musculature (treated w/patch over one eye)
  • Conjugate gaze paralysis- due to injury in fronal lobe eye field moror area (supranuclear palsy), CN 3 nulceus/nerve, gaze centers in pontine reticular formation
32
Q

Motor deficits:

A
  • Alterations in tone (flaccidity, spasticity, abnormal synergy patterns[can’t move one jt w/o entire synyergy kicking in)
  • Abnormal Reflexes (DTR, SPR, Associated reactions)
  • Decreased force production
33
Q

What is Signe Brunnstrom stages of recovery in hemiplegia?

A
  1. Flaccid Period. No mvmt of limbs elicited
  2. As recovery begins, basic limb synergies appear (associated reactions, minimal voluntary mvmt, spasticity begins to develop)
  3. Pt gains voluntary control of synergies (may not show full range of all components, spasticity increases, severe)
  4. Some mvmt combos that don’t follow synergies are mastered (spast. begins to decline)
  5. More difficult mvmt combinations and synergies decline
  6. Spast disappears and individual join mvmts become possible (coord apporaches normal)
34
Q

When is flaccidity present? How long can it last?

A

Immediately (cerebral shock). Last hours to wks. Persists in persons with damate to motor cortex and cerebellum

35
Q

characteristics of spasticity:

A
  • 90% of cases
  • Primarily in antigravity muscles (UE)
  • Can interefe with prepatory postural control (decreased balance and posture)
  • can lead to contractures
36
Q

What muscles are typically not in synergy:

A
  • Lats, teres major, Serratus ant
  • finger extensors
  • Ankle invertors
37
Q

What are DTRs like intially and post diaschesis? How do SPRs present?

A
  • DTRs
    • Initially- hypotonic
    • Post diaschesis- hypertonic
  • SPRs (babs)
    • toe flexion
    • Tonic reflex patterns (ATNR, STNR)- due to UMNL
38
Q

what are associated reactions and what are the 2 types?

A
  • unintentional mvmts ocurring when attempting to perfoan an action
  • 2 types
    • Souques phenomemon- elevating UE w/ extended elbow above horizontal results in finger ext.
    • Raimistes- resisted abduction or adduction of one LE or UE produces the same mvmt in the other.
39
Q

Which extremities and muscles are more affected with decreased force production?

A
  • UE>LE (MCA most common stroke)
  • Distal> proximal
40
Q

What impairments affect balance, gait and UE functional tasks?

A
  • Inefficient Muscle activation
  • Inability to maintain a contraction
  • Increased deffort required to produce a contraction
  • Increased reaction times
  • Increased mvmt times (effects coord.)
41
Q

What can paresis be considered?

A

An indirect impairment secondary to disuse atrophy

42
Q

Motor programming deficit in left and right hemispheres:

A
  • primarily involved in sequencing
  • Apraxia- inability to perform purposeful mvmts in absence of weakness, sensory loss, incoordination, or other factor that would explain it.
    • Ideomotor- can’t do on command but can do automatically
    • ideational- can’t do at all
43
Q

What is the dominant hemisphere for speech and language? What are 3 types of aphasia?

A
  • Left is dominant
  • 3 types of aphasia:
    • Fluent (Wernicke’s, lesion to auditory association cortex in temporal lobe, impaired auditory comprehension)
    • Nofluent (Broca’s, impaired speech w/ intact auditory comprehension, lesion to broca’s area in premotor area of frontal lobe)
    • Global (both speech and comprehension damaged)
44
Q

Perceptual dysfunctions:

A
  • primarily R hemis
  • Body Scheme disorders- disorders of a person’s internal model of the relationship of their body parts to each other and the environment
  • Body Image disorders- changes in feelings about one’s body image
45
Q

3 types of body scheme/image disorders

A
  • UL Neglect
  • Anosagnosia- lack of awareness/ denial of paretic extremities (may claim they do not belong to them)
  • Pusher syndrome- person pushes toward hemi side
46
Q

Cognitive dysfunction:

A
  • Short attention span
  • Short term memory loss- work on procedural first, then declarative
  • Perseveration- continued repetition of words or acts
47
Q

Affective disorders:

A
  • R hemis- emotional lability
  • Both hemis- depression (L>R, direct impairment)
48
Q

Behavioral changes:

A
  • Left hems- communication, difficulty processing info sequentially; seen as cautious, anxious, disorganized, hesitant to try new things
  • Right Hemis- perceptual dysfunction, can’t understand the whole idea of a task; quick, impulsive; overstimate abilities and minimize problems
49
Q

What are indirect impairments?

A
  • DVTs (biggest problem is acute phase scondary to venous statis to bedrest)
  • Skin breakdown
  • Decreased flexibility
  • Shoulder subluxation and pain
50
Q

What are halmark signs of DVT and how do you prevent it?

A
  • Signs
    • Rapid onset of UL leg swelling w/ dependent edema; may feel painful or tight; positive homan’s sign)
  • Prevention:
    • Contraction of LE
    • IPC and compression stockings
    • low-dose heparin
51
Q

How do you prevent the other indirect impairments?

A
  • Skin- avoid posn over bony prominence, inspect skin, keep dry, avoid shearing, turning schedule, use pressure limiting devices
  • Flexibility- Daily ROM, posn, resing splints
  • Shoulder- teach to be aware of own shoulder and don’t allow any pulling from caregivers
52
Q

What is the order of Rx for basic components of mvmt?

A
  1. Trunk control
  2. Midline orientation
  3. Head control on the trunk
  4. Limb function on the trunk
53
Q

How do you protect the hemi shoulder?

A
  • Never pull on the arm
  • Don’t hold on to arm for support
  • Support the weight of the arm during transfers
  • Avoid unsupported weight of the arm when positioning for lying on less involved side or when sitting in a chair
  • Avoid weight directly on arm over the point of the shoulder-protract scap
  • don’t teach self ROM
  • never use overhead trapeze
  • Beware of arm troughs and or foam wedges
54
Q
A

OSCE Neuro Remediation (5 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions